CORRIGENDUM

In the article by I. Georis, A. Feller, J. Tate, T. Cooper and E. Dubois (Genetics181:861–874) entitled “Nitrogen Catabolite Repression-Sensitive Transcription as a Readout of Tor Pathway Regulation: The Genetic Background, Reporter Gene and GATA Factor Assayed Determine the Outcomes,” strain 25T0b and all strains constructed from it (Table 1 in that article), labeled as isogenic to Sigma, are actually isogenic to S288C. The parent strain, 25T0b, emanated from the sporulation of a diploid strain isogenic to S288C [FY23 × FY73; F. Winston, C. Dollard and S. L. Ricupero-Hovasse (Yeast 11: 53–55)]. Therefore, those portions of the article addressing the resolution of the paradoxical observations obtained in TB123 vs. Sigma genetic backgrounds or mutant phenotypes reported for the Sigma genetic background are no longer valid because no Sigma strains were used in the experiments. Those data instead provide descriptions of mutant phenotypes and events occurring in the S288C genetic background. However, the overall general conclusions of the article—that the strain background, the reporter gene, and the GATA factor assayed determine the outcomes observed for Tor pathway phosphatase requirements in the regulation of NCR-sensitive gene expression—are not compromised and remain fully valid. In fact, the use of S288C, rather than of Sigma-derived strains in these experiments, intensifies the article's extended conclusion recommending consideration of these parameters when evaluating data about Tor or other regulatory pathways that influence GATA-factor-mediated gene expression.

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The Genetics Society of America (GSA), founded in 1931, is the professional membership organization for scientific researchers and educators in the field of genetics. Our members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level.